Evidence map›Paper›PMID 37353538›Full record

ArticleCommunications biology2023

Cellular senescence in white matter microglia is induced during ageing in mice and exacerbates the neuroinflammatory phenotype.

Tatsuyuki Matsudaira, Sosuke Nakano, Yusuke Konishi, Shimpei Kawamoto, Ken Uemura, Tamae Kondo, Koki Sakurai, Takaaki Ozawa, Takatoshi Hikida, Okiru Komine and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
11.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 90 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Tatsuyuki Matsudaira *Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan. matsudaira@biken.osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-2271-5317
Sosuke Nakano *Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yusuke KonishiResearch Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shimpei KawamotoResearch Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.ORCID http://orcid.org/0000-0002-7033-671X
Ken UemuraResearch Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Tamae KondoResearch Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Koki SakuraiLaboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.ORCID http://orcid.org/0000-0001-6952-7749
Takaaki OzawaLaboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.ORCID http://orcid.org/0000-0003-3633-7062
Takatoshi HikidaLaboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.ORCID http://orcid.org/0000-0002-8653-311X
Okiru KomineDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8601, Japan.ORCID http://orcid.org/0000-0003-0845-7358
Koji YamanakaDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8601, Japan.ORCID http://orcid.org/0000-0003-4655-0035
Yuki FujitaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Toshihide YamashitaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.ORCID http://orcid.org/0000-0003-4559-7018
Tomonori MatsumotoResearch Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Eiji HaraResearch Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan. ehara@biken.osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-7821-3960
The University of Osaka · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence, a state of irreversible cell-cycle arrest caused by a variety of cellular stresses, is critically involved in age-related tissue dysfunction in various organs. However, the features of cells in the central nervous system that undergo senescence and their role in neural impairment are not well understood as yet. Here, through comprehensive investigations utilising single-cell transcriptome analysis and various mouse models, we show that microglia, particularly in the white matter, undergo cellular senescence in the brain and spinal cord during ageing and in disease models involving demyelination. Microglial senescence is predominantly detected in disease-associated microglia, which appear in ageing and neurodegenerative diseases. We also find that commensal bacteria promote the accumulation of senescent microglia and disease-associated microglia during ageing. Furthermore, knockout of p16

Indexed as

MicrogliaWhite MatterAgingAnimalsCellular SenescenceMicePhenotype

Identifiers

PMID37353538
PMCPMC10290132
OpenAlexW4381839407

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.